Macdonald F, Odds F C
J Gen Microbiol. 1983 Feb;129(2):431-8. doi: 10.1099/00221287-129-2-431.
A proteinase-deficient mutant of Candida albicans, M12, was produced by nitrosoguanidine mutagenesis of a proteinase-producing strain, ATCC 28366. The mutant was phenotypically identical to its parent in nearly all biochemical and morphological characteristics except proteinase production. The mutant was considerably less lethal than the parent when inoculated intravenously into mice and lower counts of C. albicans were recovered from the organs of mice infected with the mutant. Both strains were phagocytosed and killed to a similar extent by human and murine polymorphonuclear leukocytes when the yeasts were grown in a medium that did not induce proteinase production. However, in a proteinase-inducing medium, ATCC 28366 was phagocytosed and killed less well than M12. These results indicate that proteinase secretion by C. albicans is one factor determining the virulence of the species, but that other virulence factors are also involved in the pathogenesis of systemic candidosis.
通过对产蛋白酶菌株ATCC 28366进行亚硝基胍诱变,获得了白色念珠菌的蛋白酶缺陷型突变体M12。该突变体在几乎所有生化和形态特征上与其亲本表型相同,但不产蛋白酶。将该突变体静脉注射到小鼠体内时,其致死性远低于亲本,并且从感染该突变体的小鼠器官中回收的白色念珠菌数量较少。当酵母在不诱导蛋白酶产生的培养基中生长时,两种菌株被人和鼠的多形核白细胞吞噬和杀死的程度相似。然而,在诱导蛋白酶产生的培养基中,ATCC 28366被吞噬和杀死的情况不如M12。这些结果表明,白色念珠菌分泌的蛋白酶是决定该物种毒力的一个因素,但其他毒力因子也参与了系统性念珠菌病的发病机制。